Anti-TMEM109/Mitsugumin-23 antibody

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

TMEM109 also known as Mitsugumin-23 (MG23) functions as a transmembrane protein with a mass of approximately 20-25 kDa. It resides in the endoplasmic reticulum membrane where it acts as an important component in maintaining cellular homeostasis. This protein is primarily observed across various tissues with a higher expression in muscle tissue and certain types of epithelial cells. Its structure suggests roles in calcium signaling due to domains that allow ion passage across cellular membranes.

Biological function summary

TMEM109 plays a role in the regulation of calcium ion concentrations within cells contributing to the mitochondrial permeability transition pore (MPTP) complex. This complex controls mitochondrial function by regulating the passage of ions and small metabolites which is critical for cell survival and apoptosis. Through these activities TMEM109 influences processes like muscle contraction and cell death highlighting its significance in cellular energy management and programmed cell death pathways.

Pathways

TMEM109 has roles in calcium signaling and apoptotic pathways two significant biological processes for cellular health. In the calcium signaling pathway it interacts with other proteins such as SERCA1 (Sarcoplasmic/Endoplasmic Reticulum Calcium ATPase 1) to help manage calcium ion levels within cells. In apoptotic pathways TMEM109's involvement in the MPTP complex links it to the BAX protein which is an essential regulator of apoptosis facilitating the release of cytochrome c from mitochondria triggering cascade events leading to cell death.

Associated diseases and disorders

Irregular function or expression of TMEM109 associates with conditions such as muscular dystrophy and neurodegenerative disorders. For example in muscular dystrophy altered calcium regulation and signaling through MG23 may impact muscle contraction and integrity. Additionally abnormal TMEM109 activity can connect to Alzheimer’s disease where disrupted calcium homeostasis and apoptotic signaling play roles. These disease connections make TMEM109 a considerable target for therapeutic research and intervention often intersecting pathways with proteins like dystrophin in muscular dystrophy cases and amyloid precursor protein (APP) in Alzheimer's disease.